Micro E3 Notes - History of Bacteriology Leeuwenhock...

Info iconThis preview shows page 1. Sign up to view the full content.

View Full Document Right Arrow Icon
This is the end of the preview. Sign up to access the rest of the document.

Unformatted text preview: History of Bacteriology Leeuwenhock ­ first to see bacteria (animalcules), thought bacteria came about through spontaneous generation Jenner ­ first used the word “vaccination”, used cow ­pox to produce immunity to smallpox Semmelweis ­ proposed the washing of hands in between autopsy and birth deliveries Snow ­ observed cholera in London Redi ­ worked to disprove spontaneous generation by using meat in flasks and monitoring maggot populations on them Pasteur ­ father of microbiology, disproved spontaneous generation, discovered concept of attenuation of cultures Koch ­ father of diagnostic medicine; developed staining techniques, better culture media (agar); proved germ theory Gram ­ created staining techniques (crystal violet & safranin) Bacteriology Overview Selective media ­media that inhibits some bacteria and causes others to grow Differential media ­media that causes bacteria to grow with a distinctive appearance Bacteria are prokaryotic and grow by binary division Prokaryotic Cell Structures Peptidoglycan ­structure in the outer cell wall of bacteria Transpeptidases ­enzymes that bind peptidoglycan polymers, AKA Penicillin Binding Protein (PBP) Penicillin interferes with the linkage of peptidoglycans Lysozyme degrades peptidoglycans Gram Positive Cell Walls Thick peptidoglycan layer loss of peptidoglycan results in the formation of protoplast Gram Negative Cell Walls Thin peptidoglycan layer loss of peptidoglycan results in the formation of a spheroplast Periplasmic space between the inner and outer membrane is an active metabolic area (area of virulence) Outer membrane is only found in Gram Negative bacteria Outer membrane contains LPS (Lipopolysaccharide) molecules LPS contains: Lipid A, Core polysaccharide, and O antigen Lipid A is the endotoxin that stimulates immune response (Activates B cells) Lipid A is the toxic component known as endotoxin, released when cells are disrupted/dying Endotoxic shock ­immune response to the large release of Lipid A; only occurs in Gram Negative Endotoxic shock occurs in patients with septicemia Shwartz Man Phenomenom: Disseminated Intravascular Coagulation due to tissue necrosis which occurs after second encounter with enotoxin (Lipid A) External Structures of the Bacteria Cell Flagella ( ­trichous) ­allow movement (chemo taxis) Fimbriae (pili) ­ allow adherence to host F pili (sex pili) ­only on F+ cells, one way transfer cell to cell of DNA Capsule (glycocalyx) slime layer ­ protects bacteria from antibodies/antibiotics, antiphagocytic (not picked up by neutrophils) which gives it its virulence factor and allows growth on catheters. Capsule composition ­polysaccharides help to form biofilms Structures Internal to the Bacteria Cell Bacterial chromosome ­single copy, circular, double ­stranded DNA Plasmids ­extrachromosomal DNA with the ability to replicate independentlycontain genes with virulence traits (antibiotic resistant), never contain genes for growth of the micro organism under normal conditions, transferred from one bacteria to another Endospores ­produced only by certain Gram positive species, protect chromosomal DNA of organism, Sporulation and Germination are processes to produce spores Growth Requirements Obligate aerobe ­requires oxygen Obligate anaerobe ­oxygen is toxic to bacterium Facultative anaerobe ­able to grow with or without oxygen Temperature Requirements Psychrophile ­grows best in a cold environment (0 ­20° C) Mesophile ­grows best in moderate temperature (20° ­40° C) Thermopile ­grows best in warm or hot temperature (40° ­95° C), type that infects humans Phases of Growth Lag phase ­cells are gearing up (increasing in size, synthesizing, materials for division), adjusting to growth in media Log phase ­cells are dividing, phase where antibiotics are most effective Stationary phase ­number of living and dead cells continue to increase (live=death) Death phase ­“decline” phase, cells are dying faster than growing, cells convert to spore formers Extrachromosomal DNA Plasmids ­ (discussed above) one type is F ­plasmid which is the fertility factor which allows for DNA transfer Mechanism for DNA transfer Bacteria can repair minor DNA damage Transformation ­naked DNA is picked up from the environment, Griffith determined that encapsulated smooth colonies=virulent & non ­encapsulated rough colonies=avirulent, in summary: capsule production = virulence Conjugation: one way transfer of DNA through F pilus (sex pilus), F+ is donor cell, F ­ is recipient cell Transduction ­transfer of DNA o bacteria by a virus called bacteriophage (AKA phage), recombinant bacterial cell, previous host DNA get left behind conferring new traits on the host Lysis ­replication, expression, repackaging, then release of the viral DNA with lysis of the host cell Lysogeny ­insertion of viral DNA into the host’s chromosome, dormancy then excision later (Rash of scarlet fever and diphtheria toxin due to the bacteria being lysogenized) Immunology Terminology Antigen determinant (Epitope) ­part of the antigen which antibodies bind to Compliment: C3a ­inflammation draws neutrophils C3b ­opsinization C5a ­guide neutophils(chemotaxis) Opsonization ­binding of cells (by antibodies) to make them susceptible to phagocytosis Staphlococcus Intro Catalase positive Gram + due to thick peptidoglycan layer Halophilic ­grow in high concentration of salt SIDE NOTE: Nosocomial ­hospital acquired infection Coagulase converts fibrinogesn to fibrin ­bacteria can hide from immune response in a clot Staphylococcus Aureus Naturally occurring; normal flora Has capsule (virulent, protects bacteria and adheres to host tissue) Protein A ­prevents immune recognition and clearance by macrophages(binds Fc portion of IgG) Coagulase converts fibrinogesn to fibrin ­bacteria can hide from immune response in a clot Toxins damage membranes; causes β ­hemolysis on blood agar plates 2 exfoliative toxins ­staphylococcal scalded skin syndrome and ritters disease Associated with food poisoning, toxic shock syndrome toxin (TSST ­1) Superantigens ­(Exfoliative toxin A, TSST ­1, enterotoxins) stimulate massive nonspecific and proliferation of T ­cells, cytokines are released, causing tissue damage Staph can wall itself off Enzymes associated with Staph Aureus: Coagulase ­ helps bacteria to hide in clot Catalase ­ breaks down hydrogen pyroxide (prevents bacteria from free radicals) Fibrinolysin ­ dissolves clot so bacteria can escape clot Hyaluronidase ­ allows staph aureus to spread thru tissues Lipases ­ break down lipids, essential superficial skin infections Staphlococcus Epidermis Coagulase ­negative normal flora Opportunist Major cause of sub acute Endocarditis by colonizing heart values Form biofilms on catheters, shunts, synthetic material in the body Staphylococcus Saprophyticus Coagulase Negative Normal flora Opportunist Common cause of UTI’s Staphylococcal Food Poisoning Due to intoxication by an enterotoxin(specific toxin) in G.I. tract Heat stable, acid stable Caused by either staph aureus or staph epidermis Food does not taste or smell differently Reheating food destroys bacteria, but will not inactivate the heat stable toxin Treatment ­fluid and electrolyte replacement to prevent dehydration Coagulase ­Positive Staph Infections (Staph Aureus) Be familiar with the following issues but also know that Staph can spread to various areas Impetigo ­superficial skin infection Folliculitis ­inflammation of hair follicle (sty) skin infections Carbuncles ­multiple faruncles: wound infection Bacteremia ­staph bacteria in blood Acute Endocarditis ­due to virulent bacteria due to staph in blood circulation Sub acute Endocarditis ­due to less virulent bacteria (staph epidermis) Visual indicators of Endocarditis ­Janeway Lesions, Osler’s Nodes, Petechiae Staphylococcal Pneumonia ­not common, due to inhalation of foreign material with organism Empyema ­result of pneumonia, a walled off area of consolidation in lung, “cat under the rug” on x ­ray Lung infections Osteomyelitis ­infection of the bone Brodie’s Abscess ­Osteomyelitis in long bone bone infections Septic Arthritis ­effects mechanically, abnormal joints, prosthetic joints, patients with rheumatoid arthritis (Side note: 75% of sexually active people who present with septic arthritis are infected with gonorrhea) Treatment Penicillin and methicillin ­Staph is resistant to, which has led to MRSA (Methicillin Resistance Staph Aureaus) MRSA Superbug because of its resistance, looks like strep but proceeds quicker 2 types; CA ­Community acquired (most virulent) HA ­Hospital acquired CA ­MRSA carries Pantone ­Valentin (P ­V) leukocidia thru bacteriaphage which causes severe skin, soft tissue infection & necrotizing pneumonia CA ­MRSA effects healthy individuals, HA ­MRSA effects compromised individuals CA ­MRSA presents as faruncles, deep ­seated folliculitis, impetigo, abscesses or ecthyma Spread by skin to skin contact Vancomycin is the drug of last resort prevention: hand washing Streptococcus Gram + cocci Catalase negative Hemolytic type: β ­hemolysis= complete hemolysis (clear zone around colonies) α ­hemolysis= incomplete hemolysis (green zone) γ ­hemolysis= no hemolysis (no zone) Lancefield groupings ­ originally for differentiating β ­hemolytic strains, now used to group (Group A, B,C,F,G) Streptococcus pyrogenes Group A strep pus producing Gram + Virulence factor ­ M ­proteins prevent opsonization by complement C3b (prevents C3b binding), can’t remove organism Toxins and enzymes associated with Strep pyrogenes: 1. 2. 3. 4. 5. Streptococcal pyrogenic exotoxins: cause streptococcal toxic shock syndrome and scarlet fever(erythrogenic toxin) Streptolysin S: lyses erythrocytes, leukocytes and platelets, kills phagocytic cells Streptolysin O: lyses erythrocytes, leukocytes and platelets Streptokinases: AKA fibrolysin, lyses blood clots and fibrin deposits, facilitating rapid spread of Staph pyrogenes C5a peptidases: Degrades complement molecule C5a which results in reduced chemotaxis & activation of inflammatory cells Clinal conditions with Streptococcus pyrogenes Pharyngitis (Strep throat) Scarlet fever ­ due to strains being infected by a bacteriophage resulting in lysogeny (due to erythrogenic toxin) Strep is infected by virus portion is left behind prophase codes for erythrogenic toxin produces Scarlet Fever Pyoderma ­ 2 infections, Impetigo ­ pus forming, due to infected scratch, seen in 2 ­5 year olds Erysipelas ­ red skin Cellulitis ­ involves the skin and deeper tissues Necrotizing Fasciitis ­ “flesh eating” bacteria Streptococcal toxic shock syndrome Nonsuppurative Group A strep conditions Rheumatic fever ­ occurs once strep has entered blood stream, Most common in children 5 ­15, inflammatory condition effecting cardiac, joint, vascular, subcutaneous and CNS tissues, leads to autoimmunity (molecular mimicry), can cause problems with heart valves, characterized by Aschoff bodies Acute Glomerulonephritis (AGN) ­ characterized by edema, hypertension, proteinuria, hematuria Streptococcus agalactiae Group B strep Normal Flora Colonizes in the upper respiratory and genitourinary tracts Prior cause of Puerperal sepsis which infects the baby when passed thru birth canal Most common cause of meningitis and septicemia in newborns Factors influencing colonization of the infant ­ Low birth weight, premature birth, birth trauma Risk factors for developing neonatal disease ­ above factors and lack of maternal antibody against Group B strep Viridans Streptococci Produces green pigment on blood agar opportunistic infections bacteria are found on mucous membranes Normal flora: S. sanguis ­ sticks to damaged heart valves S. mutans ­ dental caries S. bovis ­ bacteremia Streptococcus pneumoniae a viridians streptococci has a complex polysaccharide capsule Polyvalent streptococcal vaccine ­ 23 of the most common strains Nonencapsulated colonies are not virulent and are responsible for otitis media Secretory IgA protease cleaves secretory IgA found in mucous in the lungs 500,000 cases of pneumococcal pneumonia each year (along with meningitis, otitis media & sinusitis) due to pneumococcal growth. inflammatory response leads to tissue damage which results in signs and symptoms of infection S. pneumonia is found in the throat and nasopharynx of healthy individuals Enterococcus Group D Normal flora in large intestine and genitourinary tract Extreme antibiotic resistance Nosocomial infection (hospital acquired) of blood and urinary tract Previously named Streptococcus faecalis and Streptococcus faecium ...
View Full Document

This note was uploaded on 05/03/2011 for the course BIO 1 taught by Professor Paul during the Spring '11 term at Palmer Chiropractic.

Ask a homework question - tutors are online